PMID- 12832501
OWN - NLM
STAT- MEDLINE
DCOM- 20030805
LR  - 20181113
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 23
IP  - 12
DP  - 2003 Jun 15
TI  - GABA(B) receptor-mediated presynaptic inhibition has history-dependent effects on 
      synaptic transmission during physiologically relevant spike trains.
PG  - 4809-14
AB  - Presynaptic inhibition is a form of neuromodulation that interacts with 
      activity-dependent short-term plasticity so that the magnitude, and sometimes 
      even the polarity, of that activity-dependent short-term plasticity is changed. 
      However, the functional consequences of this interaction during physiologically 
      relevant spike trains are poorly understood. We examined the effects of 
      presynaptic inhibition on excitatory synaptic transmission during physiologically 
      relevant spike trains, using the GABA(B) receptor (GABA(B)R) agonist baclofen to 
      engage presynaptic inhibition and field EPSPs (fEPSPs) in hippocampal slices to 
      monitor synaptic output. We examined the effects of baclofen on the relationship 
      between an fEPSP during the spike train and the timing of spikes preceding that 
      fEPSP, a relationship that we refer to as the history dependence of synaptic 
      transmission. Baclofen alters this history dependence by causing no inhibition 
      during short interspike intervals (ISIs) in the spike train but a maximal 
      inhibition during long ISIs. This effect strengthens the dependence of the fEPSP 
      on the first ISI preceding it. One consequence of this effect is that the 
      apparent affinity of baclofen is strongly reduced during physiologically relevant 
      spike trains when compared with conventional stimulus paradigms, and a second 
      consequence is that the overall inhibition experienced by a synapse will vary 
      considerably during repeated trials of a behavioral task. We conclude that 
      GABA(B)R-mediated presynaptic inhibition is more accurately described as a 
      high-pass filter than as a simple inhibition, and that this filtering must be 
      taken into account to accurately assess the effects of presynaptic inhibition 
      under physiologically relevant conditions.
FAU - Ohliger-Frerking, Patricia
AU  - Ohliger-Frerking P
AD  - Neurological Sciences Institute, Oregon Health & Science University, Beaverton, 
      Oregon 97006, USA.
FAU - Wiebe, Sherman P
AU  - Wiebe SP
FAU - Staubli, Ursula
AU  - Staubli U
FAU - Frerking, Matthew
AU  - Frerking M
LA  - eng
GR  - R01 NS045101/NS/NINDS NIH HHS/United States
GR  - R01 NS045101-01A1/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (GABA Agonists)
RN  - 0 (GABA-B Receptor Agonists)
RN  - 0 (Receptors, GABA-B)
RN  - H789N3FKE8 (Baclofen)
SB  - IM
MH  - Action Potentials/drug effects/*physiology
MH  - Animals
MH  - Baclofen/pharmacology
MH  - Electric Stimulation/methods
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - GABA Agonists/pharmacology
MH  - GABA-B Receptor Agonists
MH  - Hippocampus/cytology/physiology
MH  - In Vitro Techniques
MH  - Neural Inhibition/drug effects/*physiology
MH  - Neurons/drug effects/metabolism/*physiology
MH  - Patch-Clamp Techniques
MH  - Presynaptic Terminals/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, GABA-B/*physiology
MH  - Synaptic Transmission/drug effects/*physiology
PMC - PMC2966496
MID - NIHMS73437
EDAT- 2003/07/02 05:00
MHDA- 2003/08/06 05:00
PMCR- 2003/12/15
CRDT- 2003/07/02 05:00
PHST- 2003/07/02 05:00 [pubmed]
PHST- 2003/08/06 05:00 [medline]
PHST- 2003/07/02 05:00 [entrez]
PHST- 2003/12/15 00:00 [pmc-release]
AID - 23/12/4809 [pii]
AID - 10.1523/JNEUROSCI.23-12-04809.2003 [doi]
PST - ppublish
SO  - J Neurosci. 2003 Jun 15;23(12):4809-14. doi: 10.1523/JNEUROSCI.23-12-04809.2003.